Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis

Atherosclerosis is a chronic lipid-driven inflammatory disease that results in the formation of lipid-rich and immune cell-rich plaques in the arterial wall, which has high morbidity and mortality in the world. The mechanism of atherosclerosis is still unclear now. Potential hypotheses involved in a...

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Main Authors: Xiaojiao Wang, Dan Luo, Sisi Wu
Format: Article
Language:English
Published: Hindawi Limited 2021-01-01
Series:Oxidative Medicine and Cellular Longevity
Online Access:http://dx.doi.org/10.1155/2021/2424509
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spelling doaj-2606f21d5b7e4b379052018c553c17022021-08-02T00:01:20ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09942021-01-01202110.1155/2021/2424509Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in AtherosclerosisXiaojiao Wang0Dan Luo1Sisi Wu2Core Facilities of West China HospitalCore Facilities of West China HospitalCore Facilities of West China HospitalAtherosclerosis is a chronic lipid-driven inflammatory disease that results in the formation of lipid-rich and immune cell-rich plaques in the arterial wall, which has high morbidity and mortality in the world. The mechanism of atherosclerosis is still unclear now. Potential hypotheses involved in atherosclerosis are chronic inflammation theory, lipid percolation theory, mononuclear-macrophage theory, endothelial cell (EC) injury theory, and smooth muscle cell (SMC) mutation theory. Changes of phospholipids, glucose, critical proteins, etc. on mitochondria-associated endoplasmic reticulum membrane (MAM) can cause the progress of atherosclerosis. This review describes the structural and functional interaction between mitochondria and endoplasmic reticulum (ER) and explains the role of critical molecules in the structure of MAM during atherosclerosis.http://dx.doi.org/10.1155/2021/2424509
collection DOAJ
language English
format Article
sources DOAJ
author Xiaojiao Wang
Dan Luo
Sisi Wu
spellingShingle Xiaojiao Wang
Dan Luo
Sisi Wu
Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis
Oxidative Medicine and Cellular Longevity
author_facet Xiaojiao Wang
Dan Luo
Sisi Wu
author_sort Xiaojiao Wang
title Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis
title_short Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis
title_full Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis
title_fullStr Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis
title_full_unstemmed Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis
title_sort molecular dysfunctions of mitochondria-associated endoplasmic reticulum contacts in atherosclerosis
publisher Hindawi Limited
series Oxidative Medicine and Cellular Longevity
issn 1942-0994
publishDate 2021-01-01
description Atherosclerosis is a chronic lipid-driven inflammatory disease that results in the formation of lipid-rich and immune cell-rich plaques in the arterial wall, which has high morbidity and mortality in the world. The mechanism of atherosclerosis is still unclear now. Potential hypotheses involved in atherosclerosis are chronic inflammation theory, lipid percolation theory, mononuclear-macrophage theory, endothelial cell (EC) injury theory, and smooth muscle cell (SMC) mutation theory. Changes of phospholipids, glucose, critical proteins, etc. on mitochondria-associated endoplasmic reticulum membrane (MAM) can cause the progress of atherosclerosis. This review describes the structural and functional interaction between mitochondria and endoplasmic reticulum (ER) and explains the role of critical molecules in the structure of MAM during atherosclerosis.
url http://dx.doi.org/10.1155/2021/2424509
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AT danluo moleculardysfunctionsofmitochondriaassociatedendoplasmicreticulumcontactsinatherosclerosis
AT sisiwu moleculardysfunctionsofmitochondriaassociatedendoplasmicreticulumcontactsinatherosclerosis
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